肿瘤相关基因Cap43在胰腺癌中的表达及意义

目的研究肿瘤相关基因Cap43在胰腺癌组织中的表达情况,探讨其对胰腺癌的诊断价值。方法收集1999年4月～2002年8月长海医院外科手术切除胰腺癌标本和癌旁正常组织33例,诊断均由病理证实。男性22例,女性11例,年龄30～73岁,平均58．1岁。所有组织标本按肿瘤、癌旁(正常)配对。采用RT-PCR和Northern杂交方法研究Cap43 mRNA表达情况。结果 RT-PCR结果显示,Cap43在肿瘤组织中表达显著上调,其在肿瘤组织和癌旁正常组织的扫描值分别为4 033±1 986和2 244±1 145,有显著差异(P<0．001)。Northern杂交亦显示Cap43在肿瘤组织中表达显著上调,相同病例的RT-PCR结果与Northern杂交的结果有较好的一致性,经回归分析,没有显著性差异(P>0．1)。结论 Cap43在胰腺癌组织中呈显著高表达,其有可能成为胰腺癌早期诊断的重要标志物。     

Place preference induced by nucleus accumbens amphetamine is impaired by antagonists of ERK or p38 MAP kinases in rats

The nucleus accumbens (NAc) plays a role in conditioned place preference (CPP). The authors tested the hypothesis that inhibition of mitogen-activated protein kinases (MAPKs) would inhibit NAc-amphetamine-produced CPP. Results confirmed that NAc amphetamine increased levels of the MAPK extracellular signal-regulated kinase (ERK). In CPP studies, NAc injections (0.5 microl per side) of the ERK inhibitor PD98059 (1.0-2.5 microg) or the p38 kinase inhibitor SB203580 (15-500 ng) dose dependently impaired CPP. The c-Jun-N-terminal kinase (JNK) inhibitor SP600125 (1.0-2.5 microg) failed to block the CPP effect. The drugs did not block amphetamine-induced motor activity. Results suggest that ERK and p38, but not JNK, MAPKs may be necessary for the establishment of NAc amphetamine-produced CPP and may also mediate other forms of reward-related learning dependent on NAc.     

Laparoscopic Right Hemicolectomy for Ileocolic Intussusception Secondary to Caecal Neoplasm

Intussusception in adults is a rare cause of abdominal pain. Unlike its paediatric counterpart, intussusception in adults is associated with obvious pathology. We describe a case of ileocolic intussusception extending to the splenic flexure. We were able to reduce the intussusception partially and pedicle was stapled carefully. The specimen was delivered through a small incision and right hemicolectomy was performed adhering to oncological principles. We recommend laparoscopic-assisted surgery is considered for adult intussusceptions.     

Nucleus accumbens PKA inhibition blocks acquisition but enhances expression of amphetamine-produced conditioned activity in rats

Rationale The nucleus accumbens (NAc) plays a central role in dopamine-produced reward-related learning. In previous studies, the cyclic adenosine monophosphate-dependent protein kinase (PKA) inhibitor Rp-Cyclic 3′,5′-hydrogen phosphorothioate adenosine triethylammonium salt (Rp-cAMPS) blocked the acquisition but not expression of NAc reward-related learning for natural rewards and the acquisition of psychostimulant drug conditioning.Objectives The current study assessed the role of PKA in the expression of NAc amphetamine (amph)-produced conditioning using conditioned activity (CA).Materials and methods After 5 days of habituation, a test environment was paired with bilateral NAc injections of amph (0.0 or 25.0 μg) and the PKA inhibitor Rp-cAMPS (0.0, 5.0, 10.0, or 20.0 μg) over three 60-min conditioning sessions separated by 48 h. To test for effects on expression, some groups received vehicle or amph alone before conditioning sessions and were injected with 0.0, 0.25, 5.0, or 20.0 μg of Rp-cAMPS before the single 60-min test session.Results Amph produced acute increases in locomotion and robust CA. Rp-cAMPS impaired the acquisition of amph-produced CA but not its expression; in fact, it enhanced expression.Conclusions Results show that PKA inhibition blocks the acquisition but not the expression of amph-produced conditioning.     

Long-term experience with implanted intrathecal drug administration systems for failed back syndrome and chronic mechanical low back pain

Background  

Continuous intrathecal drug delivery has been shown in open studies to improve pain and quality of life in those with intractable back pain who have had spinal surgery. There is limited data on long term effects and and even less for patients with mechanical back pain without prior spinal surgery.     

PAQR3: a novel tumor suppressor gene

PAQR3, also known as RKTG (Raf kinase trapping to Golgi), is a member of the progestin and adipoQ receptor (PAQR) family. The role of PAQR3 as a tumor suppressor has recently been established in different types of human cancer in which PAQR3 exerts its biological function through negative regulation of the oncogenic Raf/MEK/ERK signaling. Multiple studies have found that PAQR3 downregulation frequently occurs in human cancers and is very often associated with tumor progression and shortened patients’ survival. Moreover, restoring the expression of PAQR3 could induce apoptosis and inhibit proliferation and invasiveness of cancer cells. Downregulation of PAQR3 by oncogenic microRNAs has also been reported. In this review, we summarized current knowledge concerning the role of PAQR3 in tumor development. To our knowledge, this is the first review on the role of this novel tumor suppressor.